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Hypoxia caused by low ambient temperature leads to hypoxemia in broilers, which aggravates the metabolic burden of the liver. Liver damage is closely related to oxidative stress and apoptosis. It has been proved that taurine can reduce oxygen free radicals, exert antioxidant properties, and inhibit mitochondria-dependent apoptosis. This experiment aimed to determine whether taurine could prevent liver damage by inhibiting oxidative stress and the cytochrome c-mediated apoptotic pathway in broilers under low ambient temperature. Broilers were given 1% taurine in drinking water, and the temperature was raised at 10 °C ~ 12 °C from 21 to 42 days. At 28 and 42 days, the hepatic tissues were collected. The antioxidant capacity of liver tissues and mRNA expression levels of the factors related with cytochrome c-medicated apoptosis pathway were measured. The results showed taurine significantly increased the total antioxidant capacity (T-AOC) at 28 days. Furthermore, taurine also increased the activities of glutathione peroxidase (GSH-PX) while reducing malondialdehyde (MDA) concentration at 28 days and 42 days. Our results also revealed that taurine significantly increased the mRNA expression levels of Hsp 27 and Hsp 90 while decreasing caspase-3 mRNA expression in broiler hepatocytes at 28 days. In addition, taurine also upregulated the expression level of Bcl-2 at 42 days. In summary, the present study found that taurine enhances the antioxidant ability and alleviates cytochrome c-mediated apoptosis in hepatic tissue of broilers under low temperature.

The promotion of neurogenesis from neural stem cells (NSCs) in the hippocampus was found to be the most fundamental and effective therapy for depression. Our previous studies proved an antidepressive effect of taurine on rats, but the exact mechanism remains unclear. In this study, CUMS model was established in rats, and NSCs were cultured in vitro to investigate the protective effect and mechanisms of taurine on neurogenesis and apoptosis in CUMS rats and glutamate-injured NSCs. The results showed that ki67-positive cells were significantly increased by taurine, while apoptosis in the DG of CUMS rats was significantly inhibited by taurine. In vitro study, cell viability, Brdu

Aflatoxin B1 (AFB1) is one of the most toxic mycotoxins, which can cause serious kidney damage after ingestion. Taurine protects the kidney, an effect related to its antioxidation and anti-apoptotic actions. In the present study, taurine was administered to detect the protective effect and mechanism of taurine on AFB1-induced renal injury in rats. The results show that taurine ameliorated the increase in serum blood urea nitrogen (BUN), blood creatinine (CRE), blood uric acid (UA), cystatin c (Cys-c), and urinary protein and AKP levels. Taurine also inhibits the content of superoxide dismutase (SOD), total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px), succinate dehydrogenase (SDH), and the mRNA expression of SOD, nicotinamide adenine dinucleotide phosphate-quinine oxidoreductase 1 (NQO1), γ-glutamylcysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and glutamate cysteine ligase catalytic (GCLC) in rat kidney tissue. The apoptotic rate of renal cells was decreased by taurine through inhibition of a mitochondrial mechanism. In summary, we found that taurine prevents AFB1-induced renal injury via enhanced antioxidant ability and mitochondrial-dependent apoptosis.

Pathological cardiac hypertrophy is ultimately accompanied by cardiomyocyte apoptosis. Apoptosis mainly related to calpain-1-mediated apoptotic pathways. Studies had proved that taurine can maintain heart health through antioxidation and antiapoptotic functions, but the effect of taurine on cardiac hypertrophy is still unclear. This study aimed to determine whether taurine could inhibit calpain-1-mediated mitochondria-dependent apoptotic pathways in isoproterenol (ISO)-induced hypertrophic cardiomyocytes. We found that taurine could inhibit the increase in cell surface area and reduce the protein expression levels of the hypertrophic markers atrial natriuretic peptide, brain natriuretic polypeptide, and β-myosin heavy chain. Taurine also reduced ROS, intracellular Ca2+ overload and mitochondrial membrane potential. Moreover, taurine inhibited cardiomyocyte apoptosis by decreasing the protein expression of calpain-1, Bax, t-Bid, cytosolic cytochrome c, Apaf-1, cleaved caspase-9 and cleaved caspase-3 and by enhancing calpastatin and Bcl-2 protein expression. Calpain-1 small interfering RNA transfection results showed similar antiapoptotic effects as the taurine prevention group. However, compared with the two treatments, taurine inhibited the expression of cleaved caspase-9 more significantly. Therefore, we believe that taurine prevents ISO-induced H9c2 cardiomyocyte hypertrophy by inhibiting oxidative stress, intracellular Ca2+ overload, the calpain-1-mediated mitochondria-dependent apoptotic pathway and cleaved caspase-9 levels.

The calpain-1-activated apoptotic pathway plays a key role in right ventricular hypertrophy (RVH). Taurine has been shown to attenuate apoptosis by inhibiting calpain activity. This experiment aimed to determine whether taurine could prevent RVH by inhibiting the calpain-1/cytochrome c apoptotic pathway. The broilers were given 1% taurine dissolved in drinking water and were raised at 10 °C ~ 12 °C from day 21 to day 42. At 21 d, 28 d, 35 d and 42 d, the right ventricular (RV) tissues were collected. Increased RVH index, angiotensin II, norepinephrine and atrial natriuretic peptide mRNA expression were reduced by taurine in the broiler RVs. Taurine obviously inhibited cardiomyocyte apoptosis via maintaining the mitochondrial membrane potential and decreased the activation of caspase-9 and caspase-3 in the broiler RVs. The antioxidant assay demonstrated that taurine enhanced the activities of superoxide dismutase, total antioxidant capacity and glutathione peroxidase and the glutathione/glutathione disulfide ratio. Western blot results revealed that taurine also downregulated the expression of calpain-1 and cytosolic cytochrome c while upregulating the expression of Bcl-2/Bax and mitochondrial cytochrome c in broiler cardiomyocytes during RVH. In summary, we found that taurine could enhance cardiomyocyte antioxidant ability and further prevented cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers.

Aflatoxin B1 (AFB1), which widely exists in soil and crops, is the most toxic aflatoxin and a carcinogen to humans and animals. The liver is the main organ that processes AFB1 and other mycotoxins and is also the main target of AFB1 toxicity. Taurine is known to exhibit a variety of physiological and pharmacological functions. In the present study, taurine was administered to detect the protective effect and mechanism of taurine in AFB1-induced liver injury in rats. The results showed that taurine inhibited the increase in hepatic injury indices, hepatic apoptosis and hepatic malondialdehyde (MDA) contents while significantly enhanced the hepatic activities of antioxidant enzymes and mitochondrial function-related indices in AFB1-poisoned rats. Meanwhile, the expression levels of key factors in the Nrf2 signalling pathway were upregulated while the expression levels of key proteins in the mitochondria-mediated apoptotic pathway were downregulated after taurine administration. The results showed that taurine can reverse AFB1-induced liver injury and abnormal apoptosis through activation of the Nrf2 signalling pathway and its downstream antioxidant enzymes, which further protects mitochondria from oxidative stress and the subsequent apoptotic pathway.

Hyperuricemia can lead to direct kidney damage. Taurine participates in several renal physiological processes and has been shown as a renoprotective agent. It has been reported that taurine could reduce uric acid levels in diabetic rats, but to date there was no research on the effects of taurine on hyperuricemic rats with kidney injury. In present study, hyperuricemic rat models were induced by intragastric administration of adenine and ethambutol hydrochloride for 10 days, and taurine (1% or 2%) were added in the drinking water 7 days in advance for consecutively 17 days. The results showed that taurine alleviated renal morphological and pathological changes as well as kidney dysfunction in hyperuricemic rats. Taurine could efficiently decrease the elevated xanthine oxidase activities in hyperuricemic rats, indicating its effect on the regulation of uric acid formation. The reabsorption and secretion of uric acid are dependent on a number of urate transporters. Expressions of three urate transporters were significantly down-regulated in hyperuricemic rats, while taurine prevented the decrease of mRNA and protein expression levels of these urate transporters. The results indicate that taurine might play a role in the regulation of renal uric acid excretion. Therefore, taurine could be a promising agent for the treatment of hyperuricemia.

Excessive consumption causes alcoholic liver disease (ALD), which injures hepatocytes and induces imbalance of lipid metabolism. Taurine is known to protect the liver from various liver injuries, and relieve lipid profile. Our previous studies also found that taurine can prevent or cure ALD, reduce fat deposition, but the mechanism remains unclear. In the present study, ALD rat model was established by administration of alcohol, pyrazole and high fat diet. Two percent taurine was administered at the same time or after ALD model establishment. Serum activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), serum and hepatic TC, TG, HDL-C and LDL-C were analyzed. Real-Time RT-PCR was conducted to detect the mRNA expressions of fatty acid synthetase (FAS), acetyl-CoA catboxylase (ACC), carnitine palmitoyl transferase 1 (CPT-1), 3-Hydroxy-3-methyl glutaric acid acyl Coenzyme A reductase (HMGCR), peroxisome proliferators activated receptor α (PPARα) and sterol regulatory element-binding protein 1c (SREBP-1c). The results showed that serum ALT, AST, serum and hepatic TC, TG and LDL-C were higher, while HDL-C in ALD model rats was lower than normal rats, the changes of which can be significantly relieved by taurine administration. mRNA expressions of ACC, FAS, CPT-1, HMGCR, PPARα and SREBP-1c which were significantly changed by ethanol can also be regulated by taurine. The results indicated that taurine can prevent and repair hepatic injury of ALD rats and balance lipid metabolism indexes in the liver, the mechanisms may involves in the regulation of related enzymes and transcriptional regulators participated in lipid metabolism.

Heat stress is an environmental factor that causes severe economic loss to the current intensive breeding industry and induces huge impact on the long-term growth in livestock and poultry industry. Many animal experiments confirmed that heat stress is a major cause of heat stroke death, which is due to severe damage to endothelial cells. In order to provide a theoretical basis for the treatment or mitigation of heat stress related diseases in broilers, the effect of taurine on injury and apoptosis of aortic endothelial cells in broilers under heat stress was investigated in the present study. Ten days healthy broilers were sacrificed, then aortic tissue was used to isolate and cultivate primary broiler aortic endothelial cells. The third to the fifth generations of cells were used in the experiment. The cells were randomly divided into five groups, including control group (C), heat stress group (HS), low taurine (HS+LTau) group, mild taurine (HS+MTau) group and high taurine (HS+HTau) group. Cells in all groups were cultivated for 24 h in cell incubator (37 °C, 5% CO

It has been confirmed by our laboratory that taurine could decrease uric acid levels in hyperuricemic rats and regulate the expressions of some urate transporters. The present study aims to investigate the effects of taurine on uric acid uptake in human renal proximal tubular epithelial cells (HK-2). The cell growth inhibition rate was measured by MTS assay, which was up to 50% after treatment with 1.5 mmol/L uric acid. After administration of 15 mmol/L taurine, the inhibition rate and uric acid uptake were both significantly decreased. Then the HK-2 cells were grouped as follows: control group (C); model group (M), in which 1.5 mmol/L uric acid was added to the medium; taurine group (MT), in which 1.5 mmol/L uric acid and 15 mmol/L taurine were added to the medium; and taurine control group (T), in which 15 mmol/L taurine was added to the medium. The mRNA and protein expression levels of URAT1 and GLUT9 were measured by real-time PCR and western-blot. The results showed that URAT1 and GLUT9 mRNA/protein expression levels in group M were significantly increased compared with group C, and they were both down-regulated in MT group. In addition, the expression levels of these two transporters in group T were significantly lower than group C. The results indicated that taurine could inhibit uric acid uptake and down-regulate the expressions of URAT1 and GLUT9 in HK-2 cells.

Asthenospermia has been considered as one of the crucial causes of male infertility, which was closely related to epididymal dysfunction. Lots of documents have revealed that taurine palys an important role in male reproduction, including antioxidation, membrane stabilization, stimulation of sexual hormone secretion and elevation of sperm quality. The objective of this study was to expose the effect of taurine on spermatozoa quality and function in ornidazole-induced asthenospermia rats. We found that taurine treatment could obviously recover the decline of cauda epididymal sperm count, viability and motility, and the elevation of sperm abnormality in asthenospermia animals. Spermatozoa acrosin, LDH-X, SDH and CCO activities of model rats also were notably increased by taurine administration. The present data indicated that taurine could raise spermatozoa quality and function by elevating mitochondrial energy metabolism. Notably, taurine supplementation markedly raised serum GnRH, LH and T levels in asthenospermia rays, suggesting taurine rescued asthenosperm by means of stimulating hypothalamic-pituitary-testicular axis secretion. We also found that concentrations of asthenospermia epididymal carnitine, SA, α-Glu and ACP, and mRNA expression levels of MMP7 and IDO2 were significantly rised by taurine administration, indicating taurine may protect epididymal epithelium structure, improve secretion activity, and maintain intraluminal microenvironment homeostasis. Finally, the present results showed taurine effectively increased cauda epididymal SOD, GSH and γ-GT levels in model rats, reduced ROS and MDA production, suggesting epididymal antioxidant ability of asthenospermia rats could be elevated by taurine treatment. To sum up, our results indicated that taurine can promote spermatozoa quality and function in ornidazole-induced asthenospermia rats by facilitating epididymal epithelium secretion and luminal microenvironment homeostasis.

Objective To determine whether taurine has protective effects on chicken myocardial apoptosis induced by hypoxic condition through inhibiting calpain-1 derived mitochondrial apoptotic pathway. Methods Chicken primary embryonic myocardial cells were isolated and cultured at 37 °C under a 5% CO2 atmosphere. Firstly the optimum concentration of taurine or PD150606 was chosen by detecting the cell viability. Chicken cardiomyocytes were cultured in 95% N2-5% CO2 atmosphere for 12 h to produce hypoxic conditions. Before hypoxic treatment, 10 mM taurine and 10 uM PD150606 (a specific calpains inhibitor) were added separately or together. The cell apoptosis was detected by acridine orange/ethidium bromide (AO/EB) double staining. Western blotting was used to determine the protein expressions of calpain-1, cytochrome c, Bcl-2, procaspase-9 and procaspase-3 in the cardiomyocytes. Results Taurine administration effectively attenuated the myocardial apoptosis under hypoxic condition, reduced the calpain-1 protein level. In addition, pre-treated taurine could up-regulate the protein expressions of Bcl-2 and procaspase-3 in hypoxic myocardial cells, down-regulate protein expression levels of cytochrome c and procaspase-9. Moreover, taurine exhibited same inhibition effect as PD150606 on the cell apoptosis and proteins express under hypoxic condition. Conclusions Taurine could attenuate the chicken cardiomyocyte apoptosis impaired by hypoxia through inhibiting calpian-1-derived mitochondrial apoptotic pathway in vitro.

Asthenospermia has been considered as one of the crucial causes of male infertility, which was closely related to epididymal dysfunction. Lots of documents have revealed that taurine palys an important role in male reproduction, including antioxidation, membrane stabilization, stimulation of sexual hormone secretion and elevation of sperm quality. The objective of this study was to expose the effect of taurine on spermatozoa quality and function in ornidazole-induced asthenospermia rats. We found that taurine treatment could obviously recover the decline of cauda epididymal sperm count, viability and motility, and the elevation of sperm abnormality in asthenospermia animals. Spermatozoa acrosin, LDH-X, SDH and CCO activities of model rats also were notably increased by taurine administration. The present data indicated that taurine could raise spermatozoa quality and function by elevating mitochondrial energy metabolism. Notably, taurine supplementation markedly raised serum GnRH, LH and T levels in asthenospermia rays, suggesting taurine rescued asthenosperm by means of stimulating hypothalamic-pituitary-testicular axis secretion. We also found that concentrations of asthenospermia epididymal carnitine, SA, α-Glu and ACP, and mRNA expression levels of MMP7 and IDO2 were significantly rised by taurine administration, indicating taurine may protect epididymal epithelium structure, improve secretion activity, and maintain intraluminal microenvironment homeostasis. Finally, the present results showed taurine effectively increased cauda epididymal SOD, GSH and γ-GT levels in model rats, reduced ROS and MDA production, suggesting epididymal antioxidant ability of asthenospermia rats could be elevated by taurine treatment. To sum up, our results indicated that taurine can promote spermatozoa quality and function in ornidazole-induced asthenospermia rats by facilitating epididymal epithelium secretion and luminal microenvironment homeostasis.

Heat stress is an environmental factor that causes severe economic loss to the current intensive breeding industry and induces huge impact on the long-term growth in livestock and poultry industry. Many animal experiments confirmed that heat stress is a major cause of heat stroke death, which is due to severe damage to endothelial cells. In order to provide a theoretical basis for the treatment or mitigation of heat stress related diseases in broilers, the effect of taurine on injury and apoptosis of aortic endothelial cells in broilers under heat stress was investigated in the present study. Ten days healthy broilers were sacrificed, then aortic tissue was used to isolate and cultivate primary broiler aortic endothelial cells. The third to the fifth generations of cells were used in the experiment. The cells were randomly divided into five groups, including control group (C), heat stress group (HS), low taurine (HS+LTau) group, mild taurine (HS+MTau) group and high taurine (HS+HTau) group. Cells in all groups were cultivated for 24 h in cell incubator (37 °C, 5% CO2). Then the heat stress group cells were cultivated in a 43 °C thermostatic water bath for 6 h under heat stress, and then re-incubated under 37 °C for 1 h. The results showed that compared with the control group, expression levels of Bax, Caspase-9, Caspase-3, Cyt-c, P53 and other pro-apoptosis factors in HS groups were significantly increased (P < 0.05), while expression levels of anti-apoptosis factor Bcl-2 showed a significant decrease (P < 0.05). Compared with HS group, expression levels of Bcl-2 in endothelial cells were significantly increased by taurine administration (P < 0.05), while expression of Bax, Caspase-9, Caspase-3, Cyt-c and P53 were significantly increased by taurine (P < 0.05). In summary, the present data indicated that taurine could protect against injury and apoptosis of aortic endothelial cells under heat stress by inhibiting the activation of mitochondria-mediated apoptotic pathways.

Metabolic syndrome is a lifestyle-related disease caused by high nutrient condition and lack of exercise. The insulin resistance due to obesity has attracted attention as an underlying mechanism of metabolic syndrome. Insulin resistance refers to reduced insulin sensitivity in insulin target tissues. In this case, in order to maintain normal blood glucose levels, a compensatory large amount of insulin is released, leading to the occurrence of hyperinsulinemia. Taurine is widely distributed in animal tissues. Although it is not involved in protein synthesis, taurine plays an important role in maintaining the body's physiological function. In this experiment, insulin resistance model was induced by high fat and high sugar diet. Two percent taurine was added in drinking water to explore the mechanism of taurine in insulin resistance and to provide theoretical basis for using taurine to improve insulin resistance. The result showed that high-fat and high-sugar diet could decrease insulin sensitivity, and taurine could improve it by oral glucose tolerance test. Moreover, serum TG, TC were higher, while HDL-C in rats fed with high sugar and high fat diet was lower than normal rats, the changes of which can be significantly relieved by 2% taurine administration. mRNA and protein expressions of IRS1, and GLUT4 which were significantly changed by high sugar and high fat diet can also be regulated by 2% taurine. The results indicated that taurine can improve insulin sensitivity through remediating lipid metabolism disorder and regulating the expressions of IRS and GLUT4.

It has been confirmed by our laboratory that taurine could decrease uric acid levels in hyperuricemic rats and regulate the expressions of some urate transporters. The present study aims to investigate the effects of taurine on uric acid uptake in human renal proximal tubular epithelial cells (HK-2). The cell growth inhibition rate was measured by MTS assay, which was up to 50% after treatment with 1.5 mmol/L uric acid. After administration of 15 mmol/L taurine, the inhibition rate and uric acid uptake were both significantly decreased. Then the HK-2 cells were grouped as follows: control group (C); model group (M), in which 1.5 mmol/L uric acid was added to the medium; taurine group (MT), in which 1.5 mmol/L uric acid and 15 mmol/L taurine were added to the medium; and taurine control group (T), in which 15 mmol/L taurine was added to the medium. The mRNA and protein expression levels of URAT1 and GLUT9 were measured by real-time PCR and western-blot. The results showed that URAT1 and GLUT9 mRNA/protein expression levels in group M were significantly increased compared with group C, and they were both down-regulated in MT group. In addition, the expression levels of these two transporters in group T were significantly lower than group C. The results indicated that taurine could inhibit uric acid uptake and down-regulate the expressions of URAT1 and GLUT9 in HK-2 cells.

Taurine has been widely researched as a growth-promoting additive or as an antioxidant in aquatic animals because of its multiple functions, however, few studies have explored its effects on crustacean in spite of the occurrence of serious diseases. We studied the effects of taurine supplementation on the growth, non-specific immunity, anti-oxidative properties and gut immunity of the Chinese mitten crab Eriocheir sinensis. Healthy crabs (8.0 ± 0.5 g) were fed diets supplemented with taurine at 0% (control), 0.2%, 0.4%, 0.8%, and 1.6% for 65 days. At the end of this 65 days feeding trial, the final weight, weight gain, specific growth rate, and feed conversion ratio were best in crabs fed the 0.4% taurine diet, followed by that in those fed the 0.8% taurine diet; the parameters were worst for the control group. Carapace length (CL) and carapace width (CW) were significantly increased in the crab fed the 0.4% and 0.8% taurine diet than that of the other three groups. Total haemocyte count (THC) and acid phosphatase (ACP) activity were significantly higher in the crab fed the 0.8% taurine diet than in those belonging to the other groups, the crabs fed the 0.4% taurine diet had the highest phenoloxidase (PO), lysozyme (LZM), and alkaline phosphatase (AKP) activities, however, there was no obvious change in their haemocyanin (Hc) content. According to superoxide dismutase (SOD), glutathione Peroxidase (GSH-PX), total anti-oxidant capacity (T-AOC) activities and malondialdehyde (MDA) content, the antioxidant capacity was significantly induced by taurine diet, while was higher in crabs fed 0.4 %–0.8% taurine diet than that of the other groups. Taurine supplementation significantly up-regulated the expression of gut immune genes (EsToll2, EsRelish) and antimicrobial peptides (EsALF1, EsALF2, EsCrus1, EsCrus2) in crabs gut fed the 0.2–0.8% taurine diet group compared to control. Thus, these study results indicate that dietary taurine is important for improving growth, regulating immunity, and enhancing the antioxidant capacity in crabs, with the recommended optimum dietary allowance being 0.4 %–0.8% taurine for E. sinensis.

In males, the decline of androgen synthesis, spermatogenesis and sexual function are the main phenotypes of aging, which may be attributed to testicular dysfunction. Taurine can act as an antioxidant, a testosterone secretion stimulator, a sperm membrane stabilizer and motility factor, and an anti-apoptotic agent. Recent observational studies suggested that taurine may play an important role in spermatogenesis, but to date whether taurine has anti-aging effects on testes remains unknown. We found that in aged rats testicular SDH and G6PDH activities, marker enzymes of testes, serum testosterone, testicular 3β-HSD and 17β-HSD mRNA expression levels were significantly increased by taurine treatment. Taurine administration also markedly raised the sperm count, viability and motility, decreased the sperm abnormality. Our data suggested that taurine can postpone testicular function deterioration in aged rats. Importantly, we observed obvious elevation of testicular antioxidant enzymes (SOD, GSH, GSH-Px) activities, and remarkable reduction of ROS and MDA by taurine administration, indicating taurine can decrease testicular oxidative stress and lipid peroxidation in aged rats. Finally, we found taurine effectively reduced testicular DNA fragmentation, increased testicular Bcl-2 protein expression, and decreased cytochrome c, Bax, Fas, FasL and caspase-3 expression, suggesting taurine can prohibit aged testicular apoptosis by mitochondrial dependent and independent signal pathway. In summary, our results indicated that taurine can suppress testicular function deterioration by increasing antioxidant ability and inhibiting apoptosis.

One pathogenic mechanism of ethanol-induced liver injury is the excessive production of reactive oxygen species (ROS), which may result in alcoholic liver disease (ALD) characterized by cell death due to necrosis and apoptosis. Taurine was proved to protect against liver damage. However, whether taurine attenuates ethanol-induced hepatic apoptosis remains unknown. The present study aims to elucidate this effect and its underlying mechanism. Taurine was administered to ALD rats and an in vitro experiment in which taurine was added to primary rat hepatocytes cultured with ethanol was conducted. Mitochondrial function and anti-oxidative capacity of the liver were tested. TUNEL and AO-EB double staining were conducted to detect apoptosis of liver cells. Expressions of factors and proteins involved in mitochondrial and death receptor pathways were detected by RT-PCR and Western-blot. The results showed that taurine inhibited the decline of cell functions and apoptosis in hepatocytes cultured with ethanol. Furthermore, increased malondialdehyde (MDA) and reduced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), cytochrome c oxidase (COX) and NADH dehydrogenase (ND) in ALD rats were mediated by taurine. RT-PCR and western-blot results revealed that taurine down-regulated expression of Bax, Fas, Fas ligand (FasL), caspase 3 and caspase 9 while up-regulating the expression of Bcl-2 in ethanol-cultured hepatocytes. In summary, taurine inhibit ethanol-induced hepatic apoptosis by regulating mitochondrial or death receptor pathways.

A great deal of investigations have verified that diabetic male reproductive impairment is associated with the dysfunction of testicular steroidogenesis and spermatogenesis resulted from insulin deficiency and hyperglycaemia-induced oxidative stress. It has been identified taurine is profitable for diabetes mellitus and diabetic implications through its insulin-like and islet cells protective activity. Furthermore, our previous studies found that taurine could increase testicular antioxidative ability, stimulate the endocrine activity of hypothalamic-pituitary-testicular axis, elevate testosterone level, raise sperm quality, suppress the deterioration of testicular function. Accordingly, we hypothesized that taurine may have beneficial effects on testicular dysfunction under diabetic mellitus status. Here, we investigated the effects of taurine on testicular steroidogenesis and spermatogenesis in streptozotocin (STZ)-induced type I diabetic rats. We observed that taurine treatment can markedly increase the body and testis weights, testicular SDH and G6PDH activities, decrease the serum fasting glucose concentration of diabetic rats. Serum contents of GnRH, LH, FSH, T, and testicular StAR, 3β-HSD, 17β-HSD mRNA expression levels were also obviously raised by taurine administration, indicating that taurine can improve testicular steroidogenesis in diabetic animals. Finally, we found taurine supplementation effectively elevated the sperm count and motility, reduced sperm abnormality, suggesting that taurine can increase the testicular spermatogenesis function of diabetic rat. In summary, the present data indicated that taurine can rescue the function of testicular steroidogenesis and spermatogenesis in STZ-induced type I diabetic rats possibly by increasing the endocrine activity of hypothalamic-pituitary-testicular axis.

In order to find the effects and mechanism of taurine and L-arginine on the apoptosis of VSMCs in insulin resistance hypertensive rats.25% fructose were administered in the drinking water to Wistar rats for 12 weeks to induce the insulin resistance hypertensive model. Apoptosis of VSMCs was identified by TUNEL. The expressions of Bax protein and Bcl-2 protein were examined by immunohistochemistry.High level of fructose significantly suppressed the apoptosis of VSMCs. Taurine and L-arginine promoted apoptosis of VSMCs via increasing the Bax protein expression and decreasing the Bcl-2 protein expression.Taurine and L-arginine have obvious anti-hypertensive effects in insulin resistance hypertensive rats, and its mechanism might partially be associated with attenuating vascular remodeling by promoting apoptosis in VSMCs. In addition, the combined medication of taurine and L-arginine was more effective than single medication.

Taurine has been reported to have anti-arrhythmia effects, but the anti-atrial fibrillation (AF) effects and its mechanism remain incompletely understood. In the present study, the therapy effects and partly mechanisms were investigated. AF animal model was established by intravenous administered with the mixture of acetylcholine (Ach) and CaCl

The experiment was to elucidate protective mechanism of taurine against stress-induced hypertension. Thirty two male Wistar rats were randomly divided into four groups. Normal control group and stress control group were intragastrically administered saline; β-alanine stress group were fed with β-alanine (200 mg/kg/day) and taurine stress group with taurine (200 mg/kg/day). The hypertensive model was established by giving rats stress for 3 weeks.Results showed that significant expression levels of angiotensin converting enzyme (ACE) in the hypothalamus, pituitary and adrenal were observed in β-alanine stress group and stress control group (P0.05), but significant mRNA expression levels of angiotensin-converting enzyme 2 (ACE2) in taurine stress group and normal control group (P0.05). All the groups showed no significant differences in HSP70 mRNA expression levels in hypothalamus (P0.05), while taurine stress group exhibited the highest HSP70 mRNA expression levels both in pituitary and in adrenal (P0.05). It was also found that β-alanine stress group and stress control group had significantly higher protein expression levels of ACE in hypothalamus, pituitary and adrenal (P0.05), but significantly lower protein expression of ACE2 compared to taurine stress group and control groups (P0.05). The results indicated that taurine regulated the hypothalamus pituitary adrenal (HPA) axis of the renin-angiotensin-aldosterone system (RAAS) by inhibiting ACE gene and protein expressions and promoting ACE2 and HSP70 protein expressions, thereby contributing to the prevention of stress-induced hypertension.

Previous studies have identified that diabetic erectile dysfunction is associated with androgen and nitric oxide deficiency resulting from hyperglycemia. It has been demonstrated that taurine can stimulate testosterone secretion, increase nitric oxide synthase (NOS) activity and nitric oxide (NO) production, and reduce blood glucose levels in the diabetic animals. Furthermore, recent studies have found that taurine relaxes both the corpus cavernosum and the vasculature. Accordingly, we hypothesized that taurine might exert beneficial effects on erectile function of the diabetic rats. Here, we assessed the effects of taurine on sexual function in streptozotocin (STZ) -induced diabetic male rats. We observed that taurine treatment could markedly increase sexual response and mating ability of STZ-diabetic rats. The serum concentration of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T) were also significantly increased by taurine administration. Importantly, taurine supplementation notably increased mRNA levels and activity of endothelial NOS (eNOS) and neuronal NOS (nNOS), as well as NO and cGMP content, in the corpus cavernosum of the diabetic rats. In conclusion, the present data indicate that taurine can increase sexual function of STZ-induced diabetic male rats mainly by correcting the diabetes, increasing sexual desire, which is implicated in ameliorating the hypothalamic-pituitary-testicular axis function, and by improving penile erection, which requires increased signaling from the penile endothelial- and neuronal-dependent NO-cGMP pathway.

Taurine, a β free amino-acid, takes various biological functions including maintain the normal hepatic structure and function. In this study, the regulation mechanism of taurine on lipopolysaccharide (LPS) induced activation of Kupffer cells (KC) in the liver of rats with alcoholic liver disease (ALD) were explored. Male wistar rats were intragastrically administered with alcohol and pyrazole, and ate high-fat diet in order to establish ALD model. Taurine were administered in drinking water simultaneous with and after ALD model establishment. The preventive trial was lasted for 12 weeks, while the curative trial was lasted for 4 weeks. Finally, blood and liver were collected in order to detect the concentrations of plasma LPS and hepatic tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Hepatic total RNA were extracted, gene expressions of LPS binding protein (LBP), leukocyte differentiation antigen 14 (CD14), toll-like receptors (TLR4), nuclear transcription factor (NF-κB) and TNF-α were detected by semi-quantitative RT-PCR. The results showed significant elevated levels of plasma LPS, hepatic TNF-α, IL-1β and IL-6 in ALD rats (P0.05), and heightened gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α (P0.05); Taurine no matter administered preventively or curatively can reduce the levels of plasma LPS, hepatic TNF-α, IL-1β, IL-6, and down-regulate the gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α. The results demonstrated that taurine can prevent and cure ALD by reducing the production and transformation of LPS as well as inhibiting the opening and the transmission of LPS induced KC activation and the downstream signaling pathway.

This research aims at figure out the effects and the pathway of taurine on insulin in islet cells cultured in vitro treated by STZ. In the experiment, islet cells were isolated from pancreatic tissue by in situ perfusion with collagenase V. The pancreatic islet cells, maintained in RPMI 1640 culture medium were divided into six groups: C: control, E: supplemented with 10 mmol/L of taurine, group M, T1, T2 and T3 was treated with STZ (0.5 mmol/L), at the same time, taurine were added in group T1,T2 and T3 for 30 min, and then culture medium were collected by centrifugation and then insulin levels were detected by radioimmunoassay, the cells were then rinsed with Hanks, and 0,10, 0, 5, 10, 20 mmol/L of taurine in group C, E, M, T1, T2 and T3 were added for 24 h respectively. Total RNA was extracted, then insulin gene and its transcription regulator such as PDX-1, NeuroD1 were amplified by semi-quantitative RT-PCR. The results showed that, the release of insulin from islet cells treated by STZ could be inhibited by taurine, gene expression of insulin, PDX-1 and NeuroD1 in STZ group decreased significantly, which were up-regulated by taurine administration. In conclusion, taurine exerts a certain degree of protective and reconstructive effects on islet cells treated by STZ.

Depression, a psychiatric and dysthymic disorder, severely affects the learning, work and life quality. The main pathogenesis of depression is associated with central nervous system (CNS) dysfunction. Taurine has been demonstrated to exert protective effects on the brain development and can improve learning ability and memory. Our study investigated the antidepressant-like effects of taurine pre-treatment by examining the changes in depression-like behavior, hormones, neurotransmitters, inflammatory factors and neurotrophic factors in the hippocampus of a chronic unpredictable mild stress (CUMS)-induced depressive rat model. Taurine was found to inhibit the decrease of sucrose consumption and prevent the deficiency of spatial memory and anxiety in rats exposed to CUMS, suggesting a preventive effect of taurine on depression-like behavior. Furthermore, the decreased levels of 5-hydroxytryptamine, dopamine, noradrenaline; the increased levels of glutamate, corticosterone; and the decreased expressions of fibroblast growth factor-2, vascular endothelial growth factor and brain derived neurotrophic factor in depressive rats were hindered by taurine pre-administration. However, tumor necrosis factor-α and interleukin-1β levels were not significantly changed by taurine. The results demonstrated that the anti-depressive effect of taurine may be involved in the regulation of hypothalamic-pituitary-adrenal (HPA) axis and the promotion of neurogenesis, neuronal survival and growth in the hippocampus.

This research aims at figure out the effects and the pathway of taurine on insulin in islet cells cultured in vitro treated by STZ. In the experiment, islet cells were isolated from pancreatic tissue by in situ perfusion with collagenase V. The pancreatic islet cells, maintained in RPMI 1640 culture medium were divided into six groups: C: control, E: supplemented with 10 mmol/L of taurine, group M, T1, T2 and T3 was treated with STZ (0.5 mmol/L), at the same time, taurine were added in group T1,T2 and T3 for 30 min, and then culture medium were collected by centrifugation and then insulin levels were detected by radioimmunoassay, the cells were then rinsed with Hanks, and 0,10, 0, 5, 10, 20 mmol/L of taurine in group C, E, M, T1, T2 and T3 were added for 24 h respectively. Total RNA was extracted, then insulin gene and its transcription regulator such as PDX-1, NeuroD1 were amplified by semi-quantitative RT-PCR. The results showed that, the release of insulin from islet cells treated by STZ could be inhibited by taurine, gene expression of insulin, PDX-1 and NeuroD1 in STZ group decreased significantly, which were up-regulated by taurine administration. In conclusion, taurine exerts a certain degree of protective and reconstructive effects on islet cells treated by STZ.

Objective: In order to find the effects and mechanism of taurine and l-arginine on the apoptosis of VSMCs in insulin resistance hypertensive rats. Methods: 25% fructose were administered in the drinking water to Wistar rats for 12 weeks to induce the insulin resistance hypertensive model. Apoptosis of VSMCs was identified by TUNEL. The expressions of Bax protein and Bcl-2 protein were examined by immunohistochemistry. Results: High level of fructose significantly suppressed the apoptosis of VSMCs. Taurine and l-arginine promoted apoptosis of VSMCs via increasing the Bax protein expression and decreasing the Bcl-2 protein expression. Conclusions: Taurine and l-arginine have obvious anti-hypertensive effects in insulin resistance hypertensive rats, and its mechanism might partially be associated with attenuating vascular remodeling by promoting apoptosis in VSMCs. In addition, the combined medication of taurine and l-arginine was more effective than single medication.

A great deal of investigations have verified that diabetic male reproductive impairment is associated with the dysfunction of testicular steroidogenesis and spermatogenesis resulted from insulin deficiency and hyperglycaemia-induced oxidative stress. It has been identified taurine is profitable for diabetes mellitus and diabetic implications through its insulin-like and islet cells protective activity. Furthermore, our previous studies found that taurine could increase testicular antioxidative ability, stimulate the endocrine activity of hypothalamic-pituitary-testicular axis, elevate testosterone level, raise sperm quality, suppress the deterioration of testicular function. Accordingly, we hypothesized that taurine may have beneficial effects on testicular dysfunction under diabetic mellitus status. Here, we investigated the effects of taurine on testicular steroidogenesis and spermatogenesis in streptozotocin (STZ)-induced type I diabetic rats. We observed that taurine treatment can markedly increase the body and testis weights, testicular SDH and G6PDH activities, decrease the serum fasting glucose concentration of diabetic rats. Serum contents of GnRH, LH, FSH, T, and testicular StAR, 3β-HSD, 17β-HSD mRNA expression levels were also obviously raised by taurine administration, indicating that taurine can improve testicular steroidogenesis in diabetic animals. Finally, we found taurine supplementation effectively elevated the sperm count and motility, reduced sperm abnormality, suggesting that taurine can increase the testicular spermatogenesis function of diabetic rat. In summary, the present data indicated that taurine can rescue the function of testicular steroidogenesis and spermatogenesis in STZ-induced type I diabetic rats possibly by increasing the endocrine activity of hypothalamic-pituitary-testicular axis.

Taurine has been reported to have anti-arrhythmia effects, but the anti-atrial fibrillation (AF) effects and its mechanism remain incompletely understood. In the present study, the therapy effects and partly mechanisms were investigated. AF animal model was established by intravenous administered with the mixture of acetylcholine (Ach) and CaCl2 (66 μg/mL + 10 mg/mL) (i.v.) for 7 days. The actions of taurine (99 mg/kg∙d, introgastric administration) on the levels of Hs-CRP, IL-6, TNF-α, MMP-9, AngII, the extent of the fibrosis and ultrastructural changes in left atrial were studied. The data showed that the serum levels of TNF-α, IL-6, AngII and the plasma levels of Hs-CRP and MMP-9 were significantly elevated in automatic recovery group relative to the control group (p < 0.01), which were all decreased by taurine administration (p < 0.01) similar to Verapamil treatment. Masson’s trichrome staining of the left atrial tissue showed an obvious interstitial fibrosis in rats of automatic recovery group. The alteration could be reversed by additional taurine. Electron microscopy revealed that taurine administration could significantly alleviate the ultrastructural damage of atrial cells, and the effects were similar to the Verapamil treatment. In conclusion, the results suggested that taurine could inhibit the structural remodeling of AF in rats partly by decreasing the levels of inflammatory factors and profibrotic molecules, attenuating the extent of myocardial fibrosis and protecting the integrity of myocardial ultrastructure.

Previous studies have identified that diabetic erectile dysfunction is associated with androgen and nitric oxide deficiency resulting from hyperglycemia. It has been demonstrated that taurine can stimulate testosterone secretion, increase nitric oxide synthase (NOS) activity and nitric oxide (NO) production, and reduce blood glucose levels in the diabetic animals. Furthermore, recent studies have found that taurine relaxes both the corpus cavernosum and the vasculature. Accordingly, we hypothesized that taurine might exert beneficial effects on erectile function of the diabetic rats. Here, we assessed the effects of taurine on sexual function in streptozotocin (STZ) -induced diabetic male rats. We observed that taurine treatment could markedly increase sexual response and mating ability of STZ-diabetic rats. The serum concentration of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T) were also significantly increased by taurine administration. Importantly, taurine supplementation notably increased mRNA levels and activity of endothelial NOS (eNOS) and neuronal NOS (nNOS), as well as NO and cGMP content, in the corpus cavernosum of the diabetic rats. In conclusion, the present data indicate that taurine can increase sexual function of STZ-induced diabetic male rats mainly by correcting the diabetes, increasing sexual desire, which is implicated in ameliorating the hypothalamic-pituitary-testicular axis function, and by improving penile erection, which requires increased signaling from the penile endothelial- and neuronal-dependent NO-cGMP pathway.

The experiment was to elucidate protective mechanism of taurine against stress-induced hypertension. Thirty two male Wistar rats were randomly divided into four groups. Normal control group and stress control group were intragastrically administered saline; β-alanine stress group were fed with β-alanine (200 mg/kg/day) and taurine stress group with taurine (200 mg/kg/day). The hypertensive model was established by giving rats stress for 3 weeks.

Taurine, a β free amino-acid, takes various biological functions including maintain the normal hepatic structure and function. In this study, the regulation mechanism of taurine on lipopolysaccharide (LPS) induced activation of Kupffer cells (KC) in the liver of rats with alcoholic liver disease (ALD) were explored. Male wistar rats were intragastrically administered with alcohol and pyrazole, and ate high-fat diet in order to establish ALD model. Taurine were administered in drinking water simultaneous with and after ALD model establishment. The preventive trial was lasted for 12 weeks, while the curative trial was lasted for 4 weeks. Finally, blood and liver were collected in order to detect the concentrations of plasma LPS and hepatic tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Hepatic total RNA were extracted, gene expressions of LPS binding protein (LBP), leukocyte differentiation antigen 14 (CD14), toll-like receptors (TLR4), nuclear transcription factor (NF-κB) and TNF-α were detected by semi-quantitative RT-PCR. The results showed significant elevated levels of plasma LPS, hepatic TNF-α, IL-1β and IL-6 in ALD rats (P < 0.05), and heightened gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α (P < 0.05); Taurine no matter administered preventively or curatively can reduce the levels of plasma LPS, hepatic TNF-α, IL-1β, IL-6, and down-regulate the gene expressions of LBP, CD14, TLR4, NF-κB and TNF-α. The results demonstrated that taurine can prevent and cure ALD by reducing the production and transformation of LPS as well as inhibiting the opening and the transmission of LPS induced KC activation and the downstream signaling pathway.

Liver is considered to be the main organ capable of oxidizing alcohol and fat. Chronic consumption of alcohol is the major cause of liver injury and the development of alcoholic fatty liver disease (AFLD). Liver is also the main organ capable of synthesizing taurine, and the effects of taurine on liver disease have aroused great attention. In the present study, alcohol and pyrazole were administered to male Wistar rats by way of intragastric administration and combined with a high fat diet in order to establish the AFLD model. Taurine was administered in the drinking water during and after the establishment of the AFLD model. The preventive experiment lasted for 12 weeks. The curative experiment was divided into 4 and 8 weeks. Hepatic activities of ADH, ALDH, serum ALT, AST, TC, TG, HDL-C, LDL-C, NEFA and hepatic NEFA were measured. The results showed that hepatic ADH and ALDH in AFLD rats were significantly lower while serum ALT, AST, TC, TG, LDL-C, NEFA and hepatic NEFA in model group were significantly higher than normal rats (P < 0.05), and serum HDL-C was obviously lower. Serum ALT, AST, TC, TG, LDL-C, NEFA, and hepatic NEFA were decreased in taurine preventive and curative groups (P < 0.05), while hepatic activities of ADH and ALDH, serum HDL-C were significantly increased in taurine groups (P < 0.05). Observation of the pathological sections showed that taurine can significantly attenuate fatty degeneration and the deposition of the liver caused by alcohol. The results indicated that taurine presumably accelerates the metabolism of alcohol and fat in the liver, thereby inhibiting and reversing hepatic fatty degeneration in AFLD rats.

It is well known that there is a great amount of taurine in hypothalamus, pituitary and gonads of the mammals. Taurine plays a very important role in maintaining normal reproductive functions of mammals. However, the effects of taurine on reproductive hormone secretion in females are unclear. The experiment plans to feed rats in different estrous cycle on water containing different levels of taurine and β-alanine and test the secretion level of gonadotropin-releasing hormone (GnRH), follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), progesterone (P) and prolactin (PRL) in serum.

It has been demonstrated that taurine is abundant in male reproductive organs, and can be biosynthesized by testis, but the taurine concentration will reduce with aging. The levels of serum LH, T, NOS, and NO were found to be obviously increased by taurine supplementation in aged rats in our previous study. In addition, aging will result in a significant decline in sexual response and function, which may be attributed to the androgen deficiency. Furthermore, NO has been proposed as a crucial mediator of penile erection. That makes us hypothesize that there is potential relationship between taurine decline and erection dysfunction in aged males. So the primary aim of the present study was to investigate the effect of taurine on male sexuality in rats. Taurine was offered in water to male aged (20 months old) rats for 110 days. The effects of taurine on the sexual response, mating ability, levels of serum reproductive hormones, and penile NOS and NO levels were investigated. The results showed that taurine can significantly reduce the EL and ML; obviously increase the ERF, MF, IF, and EJF; stimulate the secretion of GnRH, LH, and T; and elevate penis NOS and NO level in aged rats. The results indicated that taurine can enhance the sexual response and mating ability in aged male rats by increasing the level of testosterone and NO, but the exact mechanism of which needs to be further investigated.

Excessive alcohol consumption is dangerous and causes serious damage to health. The main organ capable of alcohol oxidizing is liver which is also the main organ synthesizing taurine, a sulfur-containing β-amino acid, which is the major free intracellular amino acid presenting in many tissues of human and animals and exerting many physiologic and pharmacologic functions. To investigate the effect of taurine and Chinese traditional medicine on alcohol metabolism after acute alcoholic intake, male Kunming mice were administered with 60% alcohol (0.4 ml) intragastrically. Water, taurine, or taurine coadministration with Chinese traditional medicine was intragastrically administered to mice 30 min before or after alcohol intake. The disappearance of body-righting reflex was used to determine the intoxication of mice. Durations between alcohol intake and intoxication (tolerance time), intoxication and recovery (maintenance time) were recorded. The concentration of blood alcohol, levels of hepatic alcohol dehydrogenase (ADH), and acetaldehyde dehydrogenase (ALDH) were detected at 20, 50, 90, 120, and 150 min after alcohol intake. The results showed that taurine administered alone or together with Chinese traditional medicine could both significantly reduce the number of intoxicated mice, postpone the tolerance time, shorten the maintenance time, and could obvisouly decrease blood level of alcohol, increase hepatic levels of ADH and ALDH. The results indicated that taurine administered alone or together with traditional Chinese medicine could significantly accelerate the metabolism of alcohol, reduce the toxicity of alcohol, and coadministration of taurine and traditional Chinese medicine had better effects.

Taurine is the most abundant free amino acid in the human body and accounts for more than 50% of the total amino acid pool in the mammalian heart. To investigate the preventive effects of taurine on cardiac hypertrophy in rats, myocardial injury was established by hypodermic injection of isoprenaline (ISO) (10 mg/kg d) for 7 days. The preventive effects of taurine (100 mg/kg d, 200 mg/kg d, and 300 mg/kg d, i.p) on heart coefficient; ultrastructure of cardiac muscle; the levels of creatine kinase heart isoenzyme (CK-MB), cAMP, and cGMP; and antioxidant ability were investigated. The results showed that taurine could significantly prevent the increase of heart coefficient induced by ISO. Compared with the model group, 100 mg/kg and 200 mg/kg taurine significantly decrease the levels of cAMP and cGMP, while 300 mg/kg taurine could significantly decrease the levels of cAMP in myocardium, and all the three concentrations of taurine could significantly increase the ratio of cGMP/cAMP. The level of serum CK-MB was significantly increased by ISO; 200 mg/kg taurine could significantly decrease it, but 100 mg/kg and 300 mg/kg taurine had no significant effect. As for the antioxidant ability, ISO administration could significantly increase the myocardial level of MDA but had no significant effects on the myocardial levels of SOD, GSH, GSH-Px, and T-AOC. However, taurine administration could significantly decrease the myocardial level of MDA and increase the levels of GSH and T-AOC compared with the model group. The serum levels of SOD, GSH-Px, GSH, and T-AOC were significantly reduced by ISO administration, but the level of MDA showed no significant changes compared with the control group. Taurine administration could significantly increase the serum levels of SOD, GSH-Px, GSH, and T-AOC and decrease the level of MDA compared with the model group. All the results indicated that 200 mg/kg taurine had better effects. The ultrastructure of cardiomyocytes showed that taurine administration could significantly reverse the injury caused by ISO. In conclusion, the present study demonstrated that taurine could inhibit the injury induced by ISO by increasing myocardial negative inotropic effect and antioxidant ability, decreasing the hypertrophic response to isoproterenol and protecting the integrity of -myocardial ultrastructure, decreasing myocardial leak of CK-MB.

Neurogenesis has been generally accepted to happen in the subventricular zone lining the lateral ventricular and subgranular zone (SGZ) in the hippocampus of adult mammalian brain. Recent studies have reported that inflammatory stimuli, such as injection of lipopolysaccharide (LPS), impair neurogenesis in the SGZ. Taurine, a sulfur-containing β-amino acid, is a major free intracellular amino acid in many tissues of mammals and having various supplementary effects on the mammalian body functions including the brain. Recently, it has been also reported that taurine levels in the brain significantly increase under stressful conditions. The present study was aimed to evaluate the possible beneficial effects of taurine on the neurogenesis in the SGZ under the condition of acute inflammatory stimuli by LPS. Adult male rats were intraperitoneally injected with taurine once a day for 39 days. Twenty-four hours before the animals were sacrificed on the last day of taurine treatment, LPS was injected simultaneously with bromodeoxyuridine (BrdU). Immunohistochemistry for BrdU, Ki67, and Iba-1 in the brain was performed, and serum levels of TNF-α and IL-1β 2 h after LPS injection were determined. The results showed that LPS significantly decreased the number of immunoreactive cells for both BrdU and Ki67 in the SGZ, while increased that for Iba-1, all of which were restored by taurine administration. Meanwhile, the serum concentrations of TNF-α and IL-1β were significantly increased, which were significantly attenuated by taurine administration. These results suggest that taurine effectively maintains neurogenesis in the SGZ under the acute infectious condition by attenuating the increase of microgliosis in the hippocampus as well as proinflammatory cytokines in the peripheral circulation.

The present research aims to investigate the inhibition effect of taurine on the apoptosis of pancreatic islet cells induced by Streptozotocin (STZ). One hundred male Wistar rats weighing 180-200 g were randomly divided into two groups, rats in the experimental were intraperitoneally injected with 2% STZ (50 mg/kg bw, dissolved in 0.1 mmol/L pH 4.2 citrate buffer), rats in the control group were injected with the same volume of citrate buffer. Rats with the fasting blood glucose level higher than 16.7 mmol/L were selected and randomly divided into four groups: Rats in M group were STZ-induced diabetes rats, rats in T1, T2, and T3 groups were intragastrically administered with taurine (dissolved in 0.5% sodium carboxymethyl cellulose as thickening agent) once a day for 4 weeks with the contents of 0.6 g/kg, 1.2 g/kg, and 2.4 g/kg bw, respectively, while rats in group C and M were given the same amount of thickening agent as T2 group. Four weeks later, pancreatic tissues were fixed and processed for paraffin section. The results showed that STZ induced a significant increase in apoptotic rate of pancreatic islet cells, up-regulated the expression of bax and Fas and down-regulated the expression of Bcl-2, which were significantly blocked by taurine (P0.05). The results indicated that taurine could significantly restrain apoptosis of pancreatic islet cells induced by STZ.

Excessive alcohol consumption is dangerous and causes serious damage to health. The main organ capable of alcohol oxidizing is liver which is also the main organ synthesizing taurine, a sulfur-containing β-amino acid, which is the major free intracellular amino acid presenting in many tissues of human and animals and exerting many physiologic and pharmacologic functions. To investigate the effect of taurine and Chinese traditional medicine on alcohol metabolism after acute alcoholic intake, male Kunming mice were administered with 60% alcohol (0.4 ml) intragastrically. Water, taurine, or taurine coadministration with Chinese traditional medicine was intragastrically administered to mice 30 min before or after alcohol intake. The disappearance of body-righting reflex was used to determine the intoxication of mice. Durations between alcohol intake and intoxication (tolerance time), intoxication and recovery (maintenance time) were recorded. The concentration of blood alcohol, levels of hepatic alcohol dehydrogenase (ADH), and acetaldehyde dehydrogenase (ALDH) were detected at 20, 50, 90, 120, and 150 min after alcohol intake. The results showed that taurine administered alone or together with Chinese traditional medicine could both significantly reduce the number of intoxicated mice, postpone the tolerance time, shorten the maintenance time, and could obvisouly decrease blood level of alcohol, increase hepatic levels of ADH and ALDH. The results indicated that taurine administered alone or together with traditional Chinese medicine could significantly accelerate the metabolism of alcohol, reduce the toxicity of alcohol, and coadministration of taurine and traditional Chinese medicine had better effects.

Taurine is the most abundant free amino acid in the human body and accounts for more than 50% of the total amino acid pool in the mammalian heart. To investigate the preventive effects of taurine on cardiac hypertrophy in rats, myocardial injury was established by hypodermic injection of isoprenaline (ISO) (10 mg/kg d) for 7 days. The preventive effects of taurine (100 mg/kg d, 200 mg/kg d, and 300 mg/kg d, i.p) on heart coefficient; ultrastructure of cardiac muscle; the levels of creatine kinase heart isoenzyme (CK-MB), cAMP, and cGMP; and antioxidant ability were investigated. The results showed that taurine could significantly prevent the increase of heart coefficient induced by ISO. Compared with the model group, 100 mg/kg and 200 mg/kg taurine significantly decrease the levels of cAMP and cGMP, while 300 mg/kg taurine could significantly decrease the levels of cAMP in myocardium, and all the three concentrations of taurine could significantly increase the ratio of cGMP/cAMP. The level of serum CK-MB was significantly increased by ISO; 200 mg/kg taurine could significantly decrease it, but 100 mg/kg and 300 mg/kg taurine had no significant effect. As for the antioxidant ability, ISO administration could significantly increase the myocardial level of MDA but had no significant effects on the myocardial levels of SOD, GSH, GSH-Px, and T-AOC. However, taurine administration could significantly decrease the myocardial level of MDA and increase the levels of GSH and T-AOC compared with the model group. The serum levels of SOD, GSH-Px, GSH, and T-AOC were significantly reduced by ISO administration, but the level of MDA showed no significant changes compared with the control group. Taurine administration could significantly increase the serum levels of SOD, GSH-Px, GSH, and T-AOC and decrease the level of MDA compared with the model group. All the results indicated that 200 mg/kg taurine had better effects. The ultrastructure of cardiomyocytes showed that taurine administration could significantly reverse the injury caused by ISO. In conclusion, the present study demonstrated that taurine could inhibit the injury induced by ISO by increasing myocardial negative inotropic effect and antioxidant ability, decreasing the hypertrophic response to isoproterenol and protecting the integrity of -myocardial ultrastructure, decreasing myocardial leak of CK-MB.

It has been demonstrated that taurine is abundant in male reproductive organs, and can be biosynthesized by testis, but the taurine concentration will reduce with aging. The levels of serum LH, T, NOS, and NO were found to be obviously increased by taurine supplementation in aged rats in our previous study. In addition, aging will result in a significant decline in sexual response and function, which may be attributed to the androgen deficiency. Furthermore, NO has been proposed as a crucial mediator of penile erection. That makes us hypothesize that there is potential relationship between taurine decline and erection dysfunction in aged males. So the primary aim of the present study was to investigate the effect of taurine on male sexuality in rats. Taurine was offered in water to male aged (20 months old) rats for 110 days. The effects of taurine on the sexual response, mating ability, levels of serum reproductive hormones, and penile NOS and NO levels were investigated. The results showed that taurine can significantly reduce the EL and ML; obviously increase the ERF, MF, IF, and EJF; stimulate the secretion of GnRH, LH, and T; and elevate penis NOS and NO level in aged rats. The results indicated that taurine can enhance the sexual response and mating ability in aged male rats by increasing the level of testosterone and NO, but the exact mechanism of which needs to be further investigated.

Neurogenesis has been generally accepted to happen in the subventricular zone lining the lateral ventricular and subgranular zone (SGZ) in the hippocampus of adult mammalian brain. Recent studies have reported that inflammatory stimuli, such as injection of lipopolysaccharide (LPS), impair neurogenesis in the SGZ. Taurine, a sulfur-containing β-amino acid, is a major free intracellular amino acid in many tissues of mammals and having various supplementary effects on the mammalian body functions including the brain. Recently, it has been also reported that taurine levels in the brain significantly increase under stressful conditions. The present study was aimed to evaluate the possible beneficial effects of taurine on the neurogenesis in the SGZ under the condition of acute inflammatory stimuli by LPS. Adult male rats were intraperitoneally injected with taurine once a day for 39 days. Twenty-four hours before the animals were sacrificed on the last day of taurine treatment, LPS was injected simultaneously with bromodeoxyuridine (BrdU). Immunohistochemistry for BrdU, Ki67, and Iba-1 in the brain was performed, and serum levels of TNF-α and IL-1β 2 h after LPS injection were determined. The results showed that LPS significantly decreased the number of immunoreactive cells for both BrdU and Ki67 in the SGZ, while increased that for Iba-1, all of which were restored by taurine administration. Meanwhile, the serum concentrations of TNF-α and IL-1β were significantly increased, which were significantly attenuated by taurine administration. These results suggest that taurine effectively maintains neurogenesis in the SGZ under the acute infectious condition by attenuating the increase of microgliosis in the hippocampus as well as proinflammatory cytokines in the peripheral circulation.

The present research aims to investigate the inhibition effect of taurine on the apoptosis of pancreatic islet cells induced by Streptozotocin (STZ). One hundred male Wistar rats weighing 180–200 g were randomly divided into two groups, rats in the experimental were intraperitoneally injected with 2% STZ (50 mg/kg bw, dissolved in 0.1 mmol/L pH 4.2 citrate buffer), rats in the control group were injected with the same volume of citrate buffer. Rats with the fasting blood glucose level higher than 16.7 mmol/L were selected and randomly divided into four groups: Rats in M group were STZ-induced diabetes rats, rats in T1, T2, and T3 groups were intragastrically administered with taurine (dissolved in 0.5% sodium carboxymethyl cellulose as thickening agent) once a day for 4 weeks with the contents of 0.6 g/kg, 1.2 g/kg, and 2.4 g/kg bw, respectively, while rats in group C and M were given the same amount of thickening agent as T2 group. Four weeks later, pancreatic tissues were fixed and processed for paraffin section. The results showed that STZ induced a significant increase in apoptotic rate of pancreatic islet cells, up-regulated the expression of bax and Fas and down-regulated the expression of Bcl-2, which were significantly blocked by taurine (P < 0.05). The results indicated that taurine could significantly restrain apoptosis of pancreatic islet cells induced by STZ.